Article
Disease variants alter transcription factor levels and methylation of their binding sites.
Nature genetics - 1 Jan 2017
Bonder Marc Jan, Luijk René, Zhernakova Daria V, Moed Matthijs, Deelen Patrick, Vermaat Martijn, van Iterson Maarten, van Dijk Freerk, van Galen Michiel, Bot Jan, Slieker Roderick C, Jhamai P Mila, Verbiest Michael, Suchiman H Eka D, Verkerk Marijn, van der Breggen Ruud, van Rooij Jeroen, Lakenberg Nico, Arindrarto Wibowo, Kielbasa Szymon M, Jonkers Iris, van 't Hof Peter, Nooren Irene, Beekman Marian, Deelen Joris, van Heemst Diana, Zhernakova Alexandra, Tigchelaar Ettje F, Swertz Morris A, Hofman Albert, Uitterlinden André G, Pool René, van Dongen Jenny, Hottenga Jouke J, Stehouwer Coen D A, van der Kallen Carla J H, Schalkwijk Casper G, van den Berg Leonard H, van Zwet Erik W, Mei Hailiang, Li Yang, Lemire Mathieu, Hudson Thomas J, Slagboom P Eline, Wijmenga Cisca, Veldink Jan H, van Greevenbroek Marleen M J, van Duijn Cornelia M, Boomsma Dorret I, Isaacs Aaron, Jansen Rick, van Meurs Joyce B J, 't Hoen Peter A C, Franke Lude, Heijmans Bastiaan T
Abstract excerpt
Most disease-associated genetic variants are noncoding, making it challenging to design experiments to understand their functional consequences. Identification of expression quantitative trait loci (eQTLs) has been a powerful approach to infer the downstream effects of disease-associated variants, but most of these variants remain unexplained. The analysis of DNA methylation, a key component of the epigenome,...
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